The use of tissue-engineered skin to demonstrate the negative effect of CXCL5 on epidermal UV radiation-induced CPD repair efficiency.

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Ultraviolet radiation (UVR) is responsible for keratinocyte cancers (KC) through the induction of mutagenic cyclobutane pyrimidine dimers (CPDs). Many factors influence CPD repair in epidermal keratinocytes and a better understanding of those factors might lead to prevention strategies against skin cancer.The present study aims to evaluate the impact of dermal components on epidermal CPD repair efficiency and to investigate potential factors responsible for the dermal-epidermal crosstalk modulating UVR-induced DNA damage repair in keratinocytes.A model of self-assembled tissue-engineered skin containing human primary keratinocytes and fibroblasts has been used in this study.We showed that CPD repair in keratinocytes is positively influenced by the presence of a dermis. We investigated the secretome and found that the cytokine CXCL5 is virtually absent in the culture medium of reconstructed skin, when compared to media from fibroblasts and keratinocytes alone. By modulating CXCL5 levels in culture media of keratinocytes, we have shown that CXCL5 is a CPD repair inhibitor.This work outlines the impact of the secreted dermal components on epidermal UVR-induced DNA damage repair and shed light on a novel role of CXCL5 in CPD repair.


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